Suman Shankar, Sharma Pradeep Kumar, Rai Girish, Mishra Sanjay, Arora Deepika, Gupta Prachi, Shukla Yogeshwer
Proteomics & Environmental Carcinogenesis Laboratory, Food, Drug and Chemical Toxicology Group, CSIR-Indian Institute of Toxicology Research, Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, India; Academy of Scientific and Innovative Research, CSIR-IITR Campus, Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, India.
Proteomics & Environmental Carcinogenesis Laboratory, Food, Drug and Chemical Toxicology Group, CSIR-Indian Institute of Toxicology Research, Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, India; Academy of Scientific and Innovative Research, CSIR-IITR Campus, Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, India.
Biochem Biophys Res Commun. 2016 Apr 8;472(3):401-9. doi: 10.1016/j.bbrc.2015.10.133. Epub 2015 Oct 29.
Inflammation has multifaceted role in cancer progression including initiation, promotion and invasion by affecting the immune surveillance and associated signaling pathways. Inflammation facilitates the over-expression of cytokines, chemokines and growth factors involved in progression of different cancers including breast cancer progression. Deregulation of biological processes such as oxidative stress, angiogenesis, and autophagy elicit favorable immune response towards chronic inflammation. Apart from the role in carcinogenesis, chronic inflammation also favors the emergence of drug resistance clones by inducing the growth of breast cancer stem-like cells. Immunomodulation mediated by cytokines, chemokines and several other growth factors present in the tumor microenvironment regulate chronic inflammatory response and alter crosstalk among various signaling pathways such as NF-κB, Nrf-2, JAK-STAT, Akt and MAPKs involved in the progression of breast cancer. In this review, we focused on cellular and molecular processes involved in chronic inflammation, crosstalk among different signaling pathways and their association in breast cancer pathogenesis.
炎症在癌症进展中具有多方面作用，包括通过影响免疫监视及相关信号通路来启动、促进和侵袭癌症。炎症促进了参与不同癌症进展（包括乳腺癌进展）的细胞因子、趋化因子和生长因子的过度表达。诸如氧化应激、血管生成和自噬等生物过程的失调引发了针对慢性炎症的有利免疫反应。除了在致癌作用中的作用外，慢性炎症还通过诱导乳腺癌干细胞样细胞的生长，促进耐药克隆的出现。肿瘤微环境中存在的细胞因子、趋化因子和其他几种生长因子介导的免疫调节可调节慢性炎症反应，并改变参与乳腺癌进展的各种信号通路（如NF-κB、Nrf-2、JAK-STAT、Akt和MAPKs）之间的相互作用。在本综述中，我们重点关注了慢性炎症涉及的细胞和分子过程、不同信号通路之间的相互作用及其在乳腺癌发病机制中的关联。
